Diabetes is most commonly associated with aortic stiffness, but the importance of nondiabetic glucometabolic status for aortic stiffness (AS) in hypertension patients is unclear.

We included 1065 hypertension patients without diabetes in a cohort study. Carotid-femoral pulse wave velocity (cfPWV) >10 m/s can broadly be defined as AS. Pearson correlation analysis and multiple regression analysis are used to reveal the relationship between elevated fasting blood glucose (FBG) and AS.

The 1065 hypertension patients (mean age 60 years) included 48% male, 22% smokers, 94.3% with anti-hypertensive drugs, 17.9% with AS, 80% with abdominal obesity, 42% with elevated triglycerides (TG), and 27% with elevated FBG. The mean values for office systolic blood pressure (SBP)/diastolic blood pressure (DBP) and central SBP/DBP were 130/85mmHg and 132/86mmHg. Mean cfPWV was 8.7m/s. Multiple regression analysis revealed that age, office SBP, and elevated FBG were independently related to AS in the whole hypertension. Elevated FBG had 1.6-fold risk of AS in hypertension patients compared with below the cutoff. In subgroup analysis, elevated FBG increased 2.68-fold risk for AS in those without metabolic syndrome (MS), not in MS. The area under curve (AUC) of office SBP was higher than central SBP for AS in receiver operating characteristic (ROC) analysis.

We found that elevated FBG was an independent risk factor for AS in hypertension patients without MS, although there was a high proportion of abdominal obesity. Office SBP was better than central SBP to assess AS in community hypertension.

Systemic chronic inflammation may favor the onset of metabolic syndrome (MetS) which represents a risk factor for CV events. Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are disorders with high prevalence of MetS. We assessed the factors associated with MetS and its prognostic role in non-selected RA/AS/PsA patients. Between March 2014 and April 2016, 458 patients (228 RA, 134 PsA, 96 AS) selected for a primary prevention program for cardiovascular diseases were analyzed. Primary and co-primary end points were a composite of all-cause death/all-cause hospitalization and CV death/CV hospitalization, respectively. MetS was diagnosed according to the IDF Task Force on Epidemiology and Prevention. Patients were divided into MetS + (73 = 16%) and MetS - (385 = 84%). At multivariate logistic analysis, cancer, moderate/high disease activity, higher LV mass (LVM) and degree of LV diastolic dysfunction were independently associated with MetS. At 36-month follow-up, the event rate for primary/co-primary end point was 52/15% in MetS + vs 23/7% in MetS - (both p < 0.001). At multivariate Cox regression analysis, MetS was related to primary end point (HR 1.52 [CI 1.01-2.47], p = 0.04) together with higher LVM, disease duration and higher prevalence of biologic DMARDs refractoriness, and to co-primary end point (HR 2.05 [CI 1.16-3.60], p = 0.01) together with older age and higher LVM. The RA/AS/PsA phenotype MetS + is a subject with moderate/high disease activity, LV structural and functional abnormalities at increased risk for cancer. MetS + identifies RA/AS/PsA patients at higher risk for CV and non-CV events, independently of traditional CV risk factors analyzed individually and traditional indexes of inflammation.

Metabolic syndrome (MetS) is a cluster of different cardiometabolic risk factors (CMRFs), and its different combinations with other CMRFs, such as arterial stiffness have been hypothesized to explain, at least partially, increased risk of cardiovascular disease. Thus, in this systematic review and meta-analysis, we aimed to synthesize the evidence regarding the association between the clustering of MetS-related CMRFs and arterial stiffness measured using pulse wave velocity (PWV).

Original studies analysing the association between arterial stiffness, measured using PWV, and MetS were systematically searched. Pooled effect size estimates and their respective 95% confidence intervals (CI) were calculated using the DerSimonian and Laird method for two separate analyses: the diagnosis of MetS and PWV values and the number of CMRFs and PWV values.

Moderate effect size estimates were observed between MetS and PWV (0.68, 95% CI: 0.54-0.82) with a slightly higher effect size for the low-risk compared with the high-risk population group (0.75, 95% CI: 0.58-0.92; and 0.51, 95% CI: 0.32-0.82, respectively). A trend between the number of MetS-related CMRFs and PWV was found with the pooled effect size nearly doubling as the number of MetS-related CMRFs increased, 0.11 (95% CI: 0.04-0.17) for one MetS-related CMRF, 0.26 (95% CI: 0.13-0.4) for two, and 0.4 (95% CI: 0.2-0.6) for three or more.

These results demonstrated a clinically relevant association between MetS and PWV and an increasing trend in PWV values, such as a MetS-related CMRF increase. Although these results should be considered cautiously because of the considerable heterogeneity, our findings reinforce the rationale of MetS as an aggregation of risk factors with common causes, which could provide additional useful information to guide clinical management.

This review discusses sexual dimorphism in arterial stiffening, disease pathology interactions, and the influence of sex on mechanisms and pathways. Arterial stiffness predicts cardiovascular mortality independent of blood pressure. Patients with increased arterial stiffness have a 48% higher risk for developing cardiovascular disease. Like other cardiovascular pathologies, arterial stiffness is sexually dimorphic. Young women have lower stiffness than aged-matched men, but this sex difference reverses during normal aging. Estrogen therapy does not attenuate progressive stiffening in postmenopausal women, indicating that currently prescribed drugs do not confer protection. Although remodeling of large arteries is a protective adaptation to higher wall stress, arterial stiffening increases afterload to the left ventricle and transmits higher pulsatile pressure to smaller arteries and target organs. Moreover, an increase in aortic stiffness may precede or exacerbate hypertension, particularly during aging. Additional studies are needed to elucidate the mechanisms by which females are protected from arterial stiffness to provide insight into its mechanisms and, ultimately, therapeutic targets for treating this pathology.

The kidney is one of the major target organs of hypertension.Kidney damage represents a frequent event in the course of hypertension and arterial hypertension is one of the leading causes of end-stage renal disease (ESRD).ESRD has long been recognized as a strong predictor of cardiovascular (CV) morbidity and mortality. However, over the past 20 years a large and consistent body of evidence has been produced suggesting that CV risk progressively increases as the estimated glomerular filtration rate (eGFR) declines and is already significantly elevated even in the earliest stages of renal damage. Data was supported by the very large collaborative meta-analysis of the Chronic Kidney Disease Prognosis Consortium, which provided undisputable evidence that there is an inverse association between eGFR and CV risk. It is important to remember that in evaluating CV disease using renal parameters, GFR should be assessed simultaneously with albuminuria.Indeed, data from the same meta-analysis indicate that also increased urinary albumin levels or proteinuria carry an increased risk of all-cause and CV mortality. Thus, lower eGFR and higher urinary albumin values are not only predictors of progressive kidney failure, but also of all-cause and CV mortality, independent of each other and of traditional CV risk factors.Although subjects with ESRD are at the highest risk of CV diseases, there will likely be more events in subjects with mil-to-moderate renal dysfunction, because of its much higher prevalence.These findings are even more noteworthy when one considers that a mild reduction in renal function is very common in hypertensive patients.The current European Society of Hypertension (ESH)/European Society of Cardiology (ESC) guidelines for the management of arterial hypertension recommend to sought in every patient signs of subclinical (or asymptomatic) renal damage. This was defined by the detection of eGFR between 30 mL/min/1.73 m² and 60 mL/min/1.73 m² or the presence of microalbuminuria (MAU), that is an amount of albumin in the urine of 30-300 mg/day or an albumin/creatinine ratio, preferentially on morning spot urine, of 30-300 mg/g.There is clear evidence that urinary albumin excretion levels, even below the cut-off values used to define MAU, are associated with an increased risk of CV events. The relationships of MAU with a variety of risk factors, such as blood pressure, diabetes and metabolic syndrome and with several indices of subclinical organ damage, may contribute, at least in part, to explain the enhanced CV risk conferred by MAU. Nonetheless, several studies showed that the association between MAU and CV disease remains when all these risk factors are taken into account in multivariate analyses. Therefore, the exact pathophysiological mechanisms explaining the association between MAU and CV risk remain to be elucidated. The simple search for MAU and in general of subclinical renal involvement in hypertensive patients may enable the clinician to better assess absolute CV risk, and its identification may induce physicians to encourage patients to make healthy lifestyle changes and perhaps would prompt to more aggressive modification of standard CV risk factors.

Patients with metabolic syndrome (MetS) have high cardiovascular event rates. The additional effect of MetS on left ventricular (LV) systolic function in patients with type 2 diabetes mellitus (T2DM) is unknown. We studied the relation between MetS and LV systolic function in T2DM patients without coronary artery disease (CAD). Clinical and echocardiographic data from 331 T2DM patients were analyzed. Prevalence of MetS was assessed based on NCEP ATPIII definition. Stress-corrected midwall shortening (sc-MS) and mitral annular peak systolic velocity (S') were analyzed as indexes of circumferential and longitudinal shortening, respectively. Sc-MS was impaired if <89 %, S' if <8.5 cm/s (10th percentile of healthy controls). MetS was diagnosed in 172 patients. Sc-MS and S' were similar in T2DM patients with and without MetS (91 ± 14 vs 92 ± 15 %; 9.8 ± 2.0 vs 9.5 ± 2.1 cm/s, respectively; p = ns) but significantly reduced comparing to controls (102 ± 11 % and 10.8 cm/s; p < 0.0001). Impairment of sc-MS and S' were detected in 37 vs 40 % and in 29 vs 32 % of T2DM patients with and without MetS (p = ns), respectively. LV systolic function measured as sc-MS and S' is frequently impaired in T2DM patients without CAD; however, the coexistence of MetS is not associated with more severe LV systolic dysfunction. Further pathological mechanisms have to be considered to explain the negative prognostic impact of MetS in T2DM patients.

Clinical studies exploring the relationship between serum uric acid (SUA) and arterial stiffness yielded conflicting results. Only in a few of these studies, arterial distensibility was examined by measuring aortic pulse wave velocity (PWV), which is considered the gold standard for evaluating arterial stiffness. In none of the previous investigations was the influence of SUA on aortic distensibility assessed, taking into account the effect of albuminuria. The purpose of our study was to comprehensively analyse the relationships between SUA and aortic PWV in a group of essential hypertensive patients.

We enrolled 222 untreated and uncomplicated hypertensive subjects (mean age: 44 ± 10 years; 60% males), without gout. In all patients, SUA and urinary albumin excretion rate (AER) were determined. Moreover, carotid-femoral (c-f) PWV was measured. C-f PWV was significantly higher in hypertensive patients belonging to the uppermost tertile of SUA distribution, compared to subjects of the lowest tertiles (10.9 ± 2.2 vs. 10 ± 1.8 vs. 9.9 ± 1.7 m s(-1); p = 0.001). In univariate analysis, SUA correlated with c-f PWV (r = 0.24; p < 0.001). This association disappeared when AER was added in a multiple regression model, including SUA, age, mean arterial pressure, gender, metabolic syndrome components and glomerular filtration rate.

The results of our study showed that, in essential hypertensive subjects, there is a positive relationship between mild hyperuricaemia and aortic stiffness. This association weakened after adjustment for covariates and lost statistical significance after further correction for albuminuria.

Metabolic syndrome (MetS) is characterized by obesity, insulin resistance, dyslipidemia, and hypertension. The Retinal Function Imager (RFI) is a new technique for measuring retinal blood-flow velocity. This study aims to compare retinal blood flow velocity between MetS and healthy subjects.

Twenty eyes of 20 MetS males and 21 eyes of 21 aged-matched healthy males underwent RFI and carotid-femoral pulse wave velocity (PWV) measurement as well as assessment of MetS parameters. The results in MetS and healthy subjects were compared.

The average venular velocity in the MetS patients was significantly higher than in the healthy subjects (2.7 ± 0.0 mm/sec versus 2.5 ± 0.0 mm/sec respectively, P=0.013), following adjustment for age, heart rate and systolic blood pressure. Carotid-femoral PWV was higher in the MetS population than the healthy controls (10.3 ± 1.2 mm/sec versus 9.3 ± 1.5 mm/sec respectively, P=0.005). The diastolic blood pressure and MAP were correlated strongly with the arterial blood flow velocities in healthy subjects (r=0.503, P=0.020 and r=0.474, P=0.030 respectively) but not in MetS subjects.

The RFI was able to distinguish between the retinal blood flow of normal and MetS subjects. Higher venular blood flow velocity and the poor correlation between velocity and blood pressure of MetS subjects suggest that MetS causes microvascular damage.

Metabolic syndrome (MetS) is a complex condition characterized by different phenotypes, according to the combinations of risk factors and is associated with cardiovascular abnormalities. Whether control of MetS components by treatment produces improvement in the associated cardiovascular abnormalities is unknown. We investigated whether partial control of components of MetS was associated with less echocardiographic abnormalities than the complete presentation of MetS based on measured components.

We evaluated markers of echocardiographic preclinical cardiovascular disease in MetS (ATP III) defined by measured components or by history of treatment, in 1421 African-American and 1195 Caucasian non-diabetic HyperGEN participants, without prevalent cardiovascular disease or serum creatinine >2 mg/dL. Of 2616 subjects, 512 subjects had MetS by measured components and 328 by history. Hypertension was found in 16% of participants without MetS, 6% of those with MetS by history and 42% of those with MetS by measured components. Obesity and central fat distribution had similar prevalence in both MetS groups (both p < 0.0001 vs. No-MetS). Blood pressure was similar in MetS by history and No-MetS, and lower than in MetS by measured components (p < 0.0001). LV mass and midwall shortening, left atrial (LA) dimension and LA systolic force were similarly abnormal in both MetS groups (all p < 0.0001 vs. No-MetS) without difference between them.

There is a little impact of control by treatment of single components of MetS (namely hypertension) on echocardiographic abnormalities. Lower blood pressure in participants with MetS by history was not associated with substantially reduced alterations in cardiac geometry and function.

We conducted a study to evaluate arterial stiffness markers in subjects with acute ischemic stroke and metabolic syndrome and in relation to TOAST subtype of stroke. We enrolled 130 patients with acute ischemic stroke and metabolic syndrome, 127 patients with acute ischemic stroke without metabolic syndrome and 120 control subjects without acute stroke. Applanation tonometry to record pulse wave velocity (PWV). Stroke patients with metabolic syndrome, compared control subjects without stroke showed higher PWV. In subjects with ischemic stroke and metabolic syndrome, PWV was more significantly and positively correlated with body mass index, systolic blood pressure, hypertension, diabetes, glucose blood levels, LDL cholesterol levels, total cholesterol levels, micro-albuminuria, carotid plaque, previous brain infarct at neuro-imaging. Our findings underline important role of both small vessel disease and atherosclerosis on arterial stiffness pathogenesis in the clinical setting of metabolic syndrome.

To investigate the effects of amlodipine in combination with atorvastatin on carotid atherosclerotic changes in metabolic syndrome, 8-week-old Zucker fatty rats were treated with vehicle, amlodipine, atorvastatin, or amlodipine in combination with atorvastatin for 28 days. Histological studies of common carotid arteries showed that lipid deposition determined by Sudan III staining was significantly reduced in rats treated with amlodipine or atorvastatin alone and was further reduced by amlodipine in combination with atorvastatin. Immunohistochemical studies of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α, the arterial calcification initiator bone morphogenetic protein (BMP) 2, the angiogenic factor Notch1, and the smooth muscle cell marker α-smooth muscle actin (SMA) showed that the high expression of all four protein in vehicle-treated rats was greatly decreased by amlodipine, atorvastatin, or amlodipine in combination with atorvastatin, in ascending order. Double immunostaining showed marked colocalization of TNF-α with bone morphogenetic protein 2 and Notch1 with α-SMA in the vehicle group, which was greatly reduced by amlodipine plus atorvastatin. These data suggest that combination therapy may be more effective in preventing atherosclerotic processes and subsequent carotid vascular events than administrating amlodipine or atorvastatin alone in metabolic syndrome.

There is clear evidence that urinary albumin excretion levels, even below the cut-off values currently used to diagnose microalbuminuria, are associated with an increased risk of cardiovascular events. The relationships of microalbuminuria with a variety of risk factors, such as hypertension, diabetes and metabolic syndrome and with several indices of subclinical organ damage, may contribute, at least in part, to explain the enhanced cardiovascular risk conferred by microalbuminuria. Nonetheless, several studies showed that the association between microalbuminuria and cardiovascular disease remains when all these risk factors are taken into account in multivariate analyses. Therefore, the exact pathophysiological mechanisms explaining the association between microalbuminuria and cardiovascular risk remain incompletely understood. The simple search for microalbuminuria in hypertensive patients may enable the clinician to better assess absolute cardiovascular risk, and its identification may induce physicians to encourage patients to make healthy lifestyle changes and perhaps would prompt to more aggressive modification of standard cardiovascular risk factors.

The study investigates lifestyle and effective anti-hypertensive intervention in overweight-obese patients can influence insulin-resistance (HOMA-IR) and US Renal-Resistive-Index (RRI). After a 1-year interventional program (including a personalized Mediterranean diet, physical activity increase, smoking withdrawal counseling), 156 Essential Hypertension (EH) patients still have abnormal HOMA-IR, significantly higher in comparison to 159 control group patients. Body mass index (BMI) and cholesterol-high-density-lipoprotein improvement are the best predictors of a HOMA-IR decrease; RRI improves in EH according to lifestyle interventions, but no predictor to RRI is identified. Persistence of IR can be tentatively assumed as a steady sign, persistent also after extended lifestyle intervention in EH, further warranting more intensive dietary interventions.

The prevalence of cardiovascular risk factors (CRFs) has been increasing in urbanization areas of China. The article aims to estimate the up-to-date prevalence and clustering of major modifiable CRFs among suburban residents in Beijing.

A cross-sectional survey in a representative sample of 16371 suburban residents aged 35 to 74 years was carried out in 2007, and results were compared with counterparts of China and the United States. Data was collected by questionnaires, blood pressure, anthropometric, and laboratory measurements.

The age-standardized prevalence of investigated major CRFs (overweight/obesity, diabetes, hypertension, dyslipidemia, and current smoking) in the study was 36.2%, 6.5%, 36.9%, 35.4%, and 36.3%, respectively. Overall, 83.5%, 47.2% and 17.5% of participants in the study had ≥1, ≥2, and ≥3 major CRFs, which were higher than total China (80.5%, 45.9%, and 17.2%) and lower than the United State (93.1%, 73.0% and 35.9%), respectively. The adjusted odds ratio (95% confidence interval) of ≥1, ≥2, and ≥3 CRFs for men compared with women was 3.4 (3.0 to 3.9), 4.3 (3.7 to 5.0), and 5.4 (4.6 to 6.5), respectively. In addition, older age groups were more likely to have ≥1, ≥2, and ≥3 of these modifiable cardiovascular risk factors compared with younger age groups, respectively.

High prevalence and clustering of major modifiable CRFs are commonly present in suburban residents in Beijing. More effective population-based interventions, such as smoking cessation, healthy diet, increased physical activity are required to reduce the prevalence of these CRFs and the increasing burden of cardiovascular diseases in China.

There is a strong association between metabolic syndrome (MS) and increased risk of end-organ damage, cardiovascular disease, stroke, and cardiovascular mortality. Moreover, non-dipping (<10% decline in the asleep relative to the awake blood pressure [BP] mean) and elevated ambulatory pulse pressure (PP), among other factors related to the circadian BP pattern, have also been associated with increased cardiovascular morbidity and mortality. This cross-sectional study investigated the circadian BP pattern in 2,045 non-diabetic untreated patients with uncomplicated essential hypertension (941 men/1,099 women), 48.7+/-11.9 yrs of age, classified by the presence or absence of MS. BP was measured by ambulatory monitoring for 48 consecutive hours to substantiate reproducibility of the dipping pattern. Physical activity was simultaneously monitored every min by wrist actigraphy to accurately calculate mean BP when awake and asleep for each subject. MS was present in 40.7% of the patients. Patients with MS were characterized by a significantly higher 24 h mean of systolic BP and a lower diastolic BP compared to patients without MS. Accordingly, ambulatory PP was significantly elevated the entire 24 h in MS patients. The prevalence of an altered non-dipper BP profile was significantly higher in MS patients (48.4 vs. 36.1% in patients without MS, p < 0.001). MS patients were characterized, among other risk factors, by significantly higher uric acid, fibrinogen, leukocyte count, hemoglobin and globular sedimentation velocity, plus lower estimated glomerular filtration rate. Apart from corroborating the significant increased prevalence of a blunted nocturnal BP decline in MS, this study documents ambulatory PP is higher in MS, without differences between groups in mean arterial pressure. This elevated PP might reflect increased arterial stiffness in MS. MS patients were also characterized by elevated values of relevant markers of cardiovascular risk, including fibrinogen and globular sedimentation velocity. These collective findings indicate that MS should be included among the clinical situations in which ambulatory BP monitoring is recommended.

Metabolic syndrome (MetS) is associated with increased prevalence of echocardiographic LV hypertrophy (LVH), a potent predictor of cardiovascular (CV) outcome. Whether MetS increases risk of CV events independently of presence of LVH has never been investigated. It is also unclear whether LVH predicts CV risk both in the presence and absence of MetS.

Participants in the 2nd Strong Heart Study examination without prevalent coronary heart disease, congestive heart failure or renal insufficiency (plasma creatinine >2.5mg/dL) were studied (n=2758; 1746 women). MetS was defined by WHO criteria. Echocardiographic LV hypertrophy was defined using population-specific cut-point value for LV mass index (>47.3g/m(2.7)). After controlling for age, sex, LDL-cholesterol, smoking, plasma creatinine, diabetes, hypertension and obesity, participants with MetS had greater probability of LVH than those without MetS (OR=1.55 [1.18-2.04], p<0.002). Adjusted hazard of composite fatal and non-fatal CV events was greater when LVH was present, in participants without (HR=2.03 [1.33-3.08]) or with MetS (HR=1.64 [1.31-2.04], both p<0.0001), with similar adjusted population attributable risk (12% and 14%). After adjustment for LVH, risk of incident CV events remained 1.47-fold greater in MetS (p<0.003), an effect, however, that was not confirmed when diabetic participants were excluded.

LVH is a strong predictor of composite 8-year fatal and non-fatal CV events either in the presence or in the absence of MetS and accounts for a substantial portion of the high CV risk associated with MetS.

The association of aldosterone with the metabolic syndrome (MetS) has not been fully elucidated. The aim of our study was to evaluate the relationships of plasma aldosterone concentration (PAC) with MetS and left ventricular mass (LVM) in nondiabetic Caucasian patients with essential hypertension.

Measurements were taken with the patients off antihypertensive medications. The measurements included 24-h blood pressure (BP) readings, plasma renin activity (PRA) and aldosterone, and an echocardiogram.

Subjects with MetS (n = 201) had higher age-adjusted PAC (10.2 +/- 5.8 vs. 11.6 +/- 5.9 ng/dl; P = 0.01) and greater age-adjusted LVM indexed for height2.7 (LVMH2.7) (56 +/- 19 vs. 62 +/- 20 g/m2; P = 0.001) than those without MetS (n = 249). The difference in respect of PAC between the two groups was independent of PRA and was attributable mainly to obesity. After adjusting for potential confounders, LVMH2.7 was associated with MetS as a whole (beta = 0.11; P = 0.02) and with body mass index (BMI) (beta = 0.19; P < 0.0001) in the overall population. The latter relationship was attenuated (beta = 0.15; P = 0.001) after further adjustment for PAC. In the MetS group the association of LVMH2.7 with PAC held (beta = 0.19; P = 0.007) in multivariate analyses. In subjects without MetS, this relationship had only borderline statistical significance.

Our results suggest that the elevated PAC related to obesity may help to explain the increased LVM observed in association with MetS, and may contribute to enhancing the cardiovascular risk associated with MetS.

In the present study we assessed the impact of metabolic syndrome (MS) and its components on markers of cardiovascular and renal damage in a population of essential hypertensives.

A total of 651 consecutive, untreated and non-diabetic hypertensives (age 54 +/- 12 years, 340 males) who were included in the 3H Study, an ongoing registry of hypertension-related target organ damage, were considered for analysis. Left ventricular mass was indexed both for body surface area (LVMBSA) and for height2.7 (LVMheight2.7). Diastolic function was estimated by means of both conventional and tissue Doppler imaging (TDI) methods. Arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (c-f PWV) and microalbuminuria (MA) as albumin to creatinine ratio (ACR) 22-300 mg/g in men and 31-300 mg/g in women in two non-consecutive morning spot urine samples.

MS (Adult Treatment Panel III criteria) was present in 201 hypertensives (30.9%). Hypertensives with MS had increased logACR (by 10%, P = 0.01) and higher prevalence of MA (17 versus 8%, P < 0.001). Both groups exhibited similar values of LVMBSA, transmitral and TDI-derived indexes and c-f PWV (NS for all) while LVMheight2.7 was significantly higher in hypertensives with MS (by 2.6 g/m2.7, P = 0.023). Multiple regression analysis revealed that MS was an independent predictor only of logACR (beta = 0.110, P = 0.007) and MA (odds ratio = 2.577, P < 0.001), while components of blood pressure affected all studied indices of organ damage.

MS per se does not deteriorate cardiac adaptations and aortic stiffness beyond haemodynamic load in hypertension. The MS-related unfavourable effect is limited to the level of the glomerulus.

Several studies documented an association between metabolic syndrome (MetS) and left ventricular (LV) hypertrophy. However, only in a few of these studies the impact of MetS on left ventricular mass (LVM) was separately analysed by gender, with conflicting results. The aim of our study was to verify, in a wide sample of essential hypertensive patients, the influence of gender, if any, on the relationship between MetS and LVM. We enrolled 475 non-diabetic subjects (mean age: 46 +/- 11 years), with mild-to-moderate essential hypertension, of whom 40% had MetS, defined on the basis of Adult Treatment Panel III (ATPIII) criteria. All the patients underwent a 24-h ambulatory blood pressure monitoring and an echocardiogram. LVM indexed for height (2.7) (LVMH (2.7)) was significantly (P < 0.001) higher in women with MetS (n=83) than in those without it (n=97; 54+/-17 vs 42+/-11 g m(-2.7)). An equally significant difference in LVMH (2.7) was documented also in male gender between the two groups with (n=105) and without MetS (n=190; 51+/-14 vs 43+/-11 g m(-2.7); P < 0.001). The relationship between MetS and LVMH (2.7) remained statistically significant (P < 0.001) in both sexes, in multiple regression analyses, even after adjustment for potential confounding factors. Our results seem to suggest that the relationship between MetS and LVM is not significantly affected by gender, being LVM increased in both hypertensive women and men with MetS.

This cross-sectional study compared carotid artery stiffness in metabolic syndrome (MS) subjects with high-normal blood pressure (HNBP) and/or impaired glucose regulation.

Eighty-nine subjects (40M and 49F, 53.5+/-9.3 years) with either HNBP, impaired glucose regulation, or both were studied. The following measurements were included: risk factors for MS (waist circumference, blood pressure (BP), glucose, triglycerides and high-density lipoprotein (HDL) cholesterol), and carotid artery stiffness (Doppler ultrasound).

Forty-four subjects (20M and 24F) were classified as without MS (MS-) and 45 subjects (20M and 25F) as with MS (MS+). As expected, each component of MS was different between the groups (all p<0.05). Arterial distensibility in MS+ was significantly lower than in MS- (0.152+/-0.010 vs. 0.181+/-0.0091/mmHg x 10(-2), p<0.05), while beta stiffness index was not different between the two groups (12.3+/-1.1 vs. 10.5+/-1.1 AU, p=0.115). Multivariate analysis revealed that carotid artery stiffness was independently associated with resting HR together with age (both p<0.05).

These results show that, in subjects with HNBP and/or impaired glucose regulation: (1) the presence of MS decreases arterial distensibility of the carotid artery but do not increase beta stiffness index and (2) the presence of MS dose not synergistically increase carotid artery stiffness.

Increased arterial stiffness associated with diabetes and the metabolic syndrome may in part explain the increased cardiovascular disease risk observed in these conditions. Arterial stiffness can be estimated by quantifying pulse pressure but is better described by distensibility and compliance coefficients, pulse wave velocity and wave reflection. The most common non-invasive methodologies used to quantify these estimates of arterial stiffness (e.g. ultrasonography and applanation tonometry) are also described. We then review and summarise the current data on the associations between diabetes, the metabolic syndrome and insulin resistance on the one hand and greater arterial stiffness on the other, and identify and discuss some unresolved issues such as differential stiffening of central vs peripheral arterial segments, the impact of sex, and the pathobiology of increased arterial stiffness in diabetes and the metabolic syndrome. Finally, some considerations with regard to treatment options are presented. At present the most powerful therapy available for reducing arterial stiffness is to vigorously treat hypertension using pharmacological agents. New pharmacological strategies to reduce arterial stiffness are likely to be especially relevant to individuals with diabetes.

The relationships between gamma-glutamyltransferase (GGT), C-reactive protein (CRP), and arterial stiffness have not been fully investigated. The aim of this study was to clarify whether serum GGT is related to CRP and arterial stiffness estimated using brachial-ankle pulse wave velocity (baPWV).

The subjects were 3412 males and 854 females. GGT, CRP, baPWV, and conventional risk factors were evaluated. On multiple regression analysis, after adjustment for the conventional risk factors, log GGT was significantly associated with log CRP in male and female subjects (male subjects: beta=0.168, p<0.0001; female subjects: beta=0.098, p<0.05). After adjustment for the conventional risk factors, log GGT was significantly associated with PWV in male subjects (beta=0.060, p<0.0001), but in female subjects, no significant relationships were found after adjustment (beta=0.007, p=0.82).

These results suggest that GGT is independently associated with an increased level of CRP in both males and females. In addition, in males, GGT is related to an increased level of arterial stiffness.

Reduction in aortic distensibility occurs early in the atherosclerosis process and carries a poor prognosis. Metabolic syndrome is common and it is associated with increased cardiovascular mortality. The aim of this cross-sectional study was to investigate the association between metabolic syndrome and aortic distensibility.

A total of 135 subjects without diabetes were studied. Metabolic syndrome was diagnosed using the NCEP-ATP-III criteria. Aortic distensibility was assessed non-invasively by ultrasonography. Multivariate analysis, after controlling for the components of the metabolic syndrome, and, additionally, for body mass index, pulse pressure, presence of coronary artery disease, use of statins and use of angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers, demonstrated an independent association between aortic distensibility and age (p<0.001), systolic blood pressure, (p=0.02), diastolic blood pressure (p=0.005), and history of hypertension (p<0.001), but not metabolic syndrome status. Moreover, there was a suggestive association with albumin-to-creatinine ratio (p=0.06).

Metabolic syndrome per se is not associated with reduction in aortic distensibility. From the components of the metabolic syndrome, only blood pressure is a strong predictor of aortic distensibility. In addition, ageing and higher values of albumin-to-creatinine ratio are also associated with low aortic distensibility.

The aim of the study was to cross-sectionally analyze, in a group of essential hypertension patients without diabetes mellitus, the influence of the metabolic syndrome (MS) on the stroke volume index to pulse pressure (SVi/PP) ratio, a measure of total arterial compliance. A total of 528 essential hypertension patients, aged 18 to 72 years, free from cardiovascular and renal disease (41% of whom had MS) were enrolled. All participants underwent routine blood chemistry, echocardiographic examination, and 3 blood pressure measurements at the end of echocardiographic examination. When compared with participants who did not have MS, hypertensive patients with MS exhibited lower SVi/PP ratio (0.65+/-0.22 vs 0.73+/-0.21 mm Hg; P=.0003). The independent association of MS with SVi/PP ratio (beta=0.10; P=.02) was confirmed in a multivariate regression model including age, sex, and other potential confounders as covariates. The authors' finding may help to explain the enhanced cardiovascular risk associated with MS.

The aim of this study was to evaluate the impact of the metabolic syndrome (MS) and its components as defined by the National Cholesterol Education Program Adult Treatment Panel III on arterial stiffness in untreated hypertensive patients.

This was a cross sectional multi-center study performed in 46 healthcare centers, from 14 countries involved in the Complior study. Four hundred and forty patients (55% male) aged 18-73 years, with untreated essential hypertension were selected at inclusion. All patients underwent a full evaluation for all the risk factors representing the MS and an assessment of arterial stiffness using automatic measurement of carotid-femoral pulse wave velocity (PWV).

In the overall population significant correlations were found, respectively, between PWV, MS (R=0.2, P<0.001) and gender (R=0.11, P=0.023) where PWV was higher in women. After adjustment for age and systolic blood pressure (SBP), analysis of covariance showed an independent effect of the MS on PWV, this effect increased with ageing and SBP especially after 47 years (age median, P=0.0047). Moreover, increase of mean PWV was highly associated with the number of MS factors in global population (P<0.001). These findings suggest that MS leads to early arterial wall ageing.

Presence of MS induces an increase of arterial stiffness in untreated hypertensive patients independently from age and SBP. The increase of PWV is proportional to number of risk factors and affects principally patients after mid-age of 47 years where MS has ageing effects on arterial stiffness.

The relation of metabolic syndrome (MetS) with cardiovascular outcome may be less evident when preclinical cardiovascular disease is present. We explored, in a post hoc analysis, whether MetS predicts cardiovascular events in hypertensive patients with electrocardiographic left ventricular hypertrophy (ECG-LVH) in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. MetS was defined by >or=2 risk factors plus hypertension: body mass index >or=30 kg/m(2), high-density lipoprotein (HDL)-cholesterol <1.0/1.3 mmol/l (<40/50 mg/dl) (men/women), glucose >or=6.1 mmol/l (>or=110 mg/dl) fasting or >or=7.8 mmol/l (>or=140 mg/dl) nonfasting or diabetes. Cardiovascular death and the primary composite end point (CEP) of cardiovascular death, stroke and myocardial infarction were examined. In MetS (1,591 (19.3%) of 8,243 eligible patients), low HDL-cholesterol (72%), obesity (77%) and impaired glucose (73%) were similarly prevalent, with higher blood pressure, serum creatinine and Cornell product, but lower Sokolow-Lyon voltage (all P<0.001). After adjusting for baseline covariates, hazard ratios for CEPs and cardiovascular death (4.8+/-1.1 years follow-up) were 1.47 (95% confidence interval (CI), 1.27-1.71)- and 1.73 (95% CI, 1.38-2.17)-fold higher with MetS (both P<0.0001), and were only marginally reduced when further adjusted for diabetes, obesity, low HDL-cholesterol, non-HDL-cholesterol, pulse pressure and in-treatment systolic blood pressure and heart rate. Thus, MetS is associated with increased cardiovascular events in hypertensive patients with ECG-LVH, independently of single cardiovascular risk factors.

This study aimed to investigate whether the clustering of the risk factors of the metabolic syndrome (MetS) is associated with stiffness of central and peripheral arterial segments; whether these associations are similar in men and women; and whether insulin resistance and low-grade inflammation mediate any such associations.

Increased arterial stiffness may explain, at least in part, the increased cardiovascular and diabetes risk associated with the MetS. However, the mechanisms linking the MetS to an increased arterial stiffness are incompletely understood, and gender differences may exist.

Cross-sectional analyses of data on 313 young men and women (mean age 23 years) from the Northern Ireland Young Hearts Project. Subjects were categorized according to the number of traits of the MetS; in addition a continuous MetS score was calculated. Arterial stiffness was assessed by measuring pulse wave velocity (PWV) in three arterial segments using a non-invasive optical method.

The prevalence of the MetS was similar for men (10.6%) and women (10.5%). After adjustment for potential confounders and other cardiovascular risk factors, PWV of the three arterial segments investigated increased with increasing traits of the MetS in women only. Women with the MetS, as compared to those without risk factors of the syndrome, had greater PWV of the aorto-iliac (+14.0%, P = 0.016), the aorto-radial (+13.2%, P = 0.010) and aorto-dorsalis pedis (+11.8%, P = 0.011) segments. A great deal (up to 75%) of the association between the MetS and aortic-iliac PWV was mediated by heart rate, inflammation markers [C-reactive protein (CRP) and fibrinogen] and insulin resistance [homeostatic model assessment-insulin resistance (HOMA-IR)], whereas these variables did not explain much of the association between the MetS and PWV of the peripheral segments.

Young women with the MetS show increased stiffness of peripheral and central arteries, a mechanism that may explain their increased cardiovascular risk. Low-grade inflammation, insulin resistance and sympathetic activation explain much of the adverse impact of the MetS on central, but not peripheral, arterial stiffness.

Metabolic syndrome (MS) has been associated with an increased left ventricular (LV) mass in recent reports. Little is known about the association of MS with LV mass (LVM) in overweight and obese individuals. The aim of our study was to investigate the relation between MS and LVM in a population of overweight and obese hypertensive subjects.

289 non-diabetic essential hypertensives with a body mass index >25 kg/m2, were enrolled. In all subjects routine blood chemistry, echocardiographic examination and 24-h ambulatory blood pressure monitoring were performed.

In the group of overweight patients, participants with MS (n=58), when compared to those without it (n=127), exhibited significantly greater LVM indexed for height(2.7) (LVMH(2.7)) (50+/-12 vs 44+/-11 g/m(2.7); p=0.0001), even after controlling for age, gender and 24-h systolic blood pressure. Similar results were obtained in the group of obese individuals, being LVMH(2.7) (56+/-12 vs 44+/-9 g/m(2.7); p<0.0001) greater in subjects with MS (n=77) than in those without MS (n=27), even after adjustment for age, gender and clinic systolic blood pressure. The independent association of MS with LVMH(2.7) in overall study population was confirmed by linear multiple regression analyses (beta=0.20; p=0.0004).

MS seems to increase LVM over and above the potential contribution of blood pressure, body size and other single components of this syndrome. Since LV hypertrophy is a well-known predictor of cardiovascular events, our results may partly explain the enhanced cardiovascular risk associated with MS.

High blood pressure is often associated with various metabolic abnormalities, including abdominal obesity, dyslipidemia, elevated plasma glucose, and insulin resistance, which are the main features of the metabolic syndrome. The metabolic syndrome is extremely common worldwide. This high prevalence is of considerable concern because several studies suggest that the metabolic syndrome carries an increased risk for cardiovascular events. Several lines of evidence seem to indicate that the metabolic syndrome is associated with an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, microalbuminuria, impaired aortic elasticity, and early carotid atherosclerosis, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. It is conceivable that these data may partly explain the high rates of cardiovascular morbidity and mortality that are observed in patients with the metabolic syndrome.